We then characterized spatial patterns in the density of per capita contact rates of simulated raccoons.
For the C1 light-modulatable histidine protein kinase we then characterized the kinetic basis of its light sensitivity.
We then characterized the surfaces with an optical profilometer, a scanning electron microscope and contact angle measurements.
We then characterized traveling behavior at the level of the individual using hidden Markov models (HMMs) constructed from the experimental data.
We then characterized a mixed dimer variant in which one chain contained an E371A substitution (which prevents binding of the substrate l-arginine) while the other subunit was left unaltered.
We then characterized RUNX1 protein expression by Western blot analysis.
We then characterized NK1-R expression in the superficial dorsal horn rostrocaudally along the lumbar segment.
Using an optimized DNCB sensitization scheme (Figure 1A), we then characterized the pathogenic changes in the back and ear skins.
We then characterized these transgenic mice behaviorally to investigate the role of adult neurogenesis in hippocampal-dependent spatial learning.
In light of the beneficial role of Gag-specific CTL responses, we then characterized patterns of genetic variation in Gag sequences, particularly those linked to HLA-mediated mutations.
We identified an embryonic stem (ES) cell line with an EpCAM (tacstd1) mutation created by gene trapping, and used it to generate EpCAM-knockout mice which we then characterized.
